Effect of Treatment with Recombinant Human Erythropoietin on Peripheral Hemodynamics and Oxygenation

Nonnast-Daniel, B.; Creutzig, A; Kuhn, Katja E.; Bahlmann, J.; Reimers, Emilio González; Brunkhorst, R.; Caspary, L; Koch, K. M.

doi:10.1159/000416017

Cited by 67 publications

(31 citation statements)

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“…When stimulated by vasoactive agents such as acetylcholine or by increased shear stress, mechanism by which TPR may increase with correction of the anemia is via the reversal of hypoxic vasodilatation endothelial cells produce an endothelial factor identified as nitric oxide (NO). The release of endogenous NO from following improved tissue oxygenation [31]. The observation that EPO therapy can induce hypertension without endothelial cells tonically reduces the peripheral vascular resistance and BP.…”

Section: Arginine Vasopressin Erythropoietinmentioning

confidence: 99%

Hypertension in Dialysis Patients

Bellinghieri

Santoro²,

Mazzaglia³

et al. 1999

Mineral Electrolyte Metab

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Hypertension is a major risk for cardiovascular complications in dialysis patients. The pathogenesis of hypertension is multifactorial and is not completely understood. Hypervolemia has always been considered a major pathogenetic factor. In addition, a disturbed hormone profile with an activated renin angiotensin system, increased catecholamine, vasopressin and endothelin, and perhaps decreased nitrous oxide activity seem to play a role in the high incidence of hypertension in dialysis patients. The influence of autonomic dysfunction on blood pressure control in hemodialysis patients is not clear. The frequent use of erythropoietin during the last decade may have contributed to the increased incidence of hypertension in the dialysis population. Data from the First Report on Dialysis and Transplant in Sicily showed that hypertension is the cause of end-stage renal disease in 8% of dialysis patients and that the incidence of hypertension, as a cause of end-stage renal disease, increased with age.

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Section: Arginine Vasopressin Erythropoietinmentioning

confidence: 99%

Hypertension in Dialysis Patients

Bellinghieri

Santoro²,

Mazzaglia³

et al. 1999

Mineral Electrolyte Metab

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“…It had been proposed that tissue protection and repair associated with EPO depends upon a heteromeric receptor composed of EPO receptor subunits complexed with the beta common receptor (CD131) also used by other type I cytokines, resulting in activation of a whole array of antiapoptotic and antiinflammatory pathways (Brines et al, 2004). However, due to its erythropoietic potency, which has made EPO so useful for treatment of anemia, and due to increased risk of thrombosis (Wolf et al, 1997a,b;Stohlawetz et al, 2000;Haiden et al, 2005;Stasko et al, 2007;Kirkeby et al, 2008;Kato et al, 2010) and hypertension (Nonnast-Daniel et al, 1988;Schaefer et al, 1988;Vaziri, 1999), continuous EPO administration is unacceptable for treatment of CHF. Even a single dose of recombinant human EPO (rhEPO), in fact, can be associated with undesirable increases in platelet activation and number (Lippi et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Chronic Administration of Small Nonerythropoietic Peptide Sequence of Erythropoietin Effectively Ameliorates the Progression of Postmyocardial Infarction–Dilated Cardiomyopathy

Ahmet

Tae

Brines

et al. 2013

J Pharmacol Exp Ther

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The cardioprotective properties of erythropoietin (EPO) in preclinical studies are well documented, but erythropoietic and prothrombotic properties of EPO preclude its use in chronic heart failure (CHF). We tested the effect of long-term treatment with a small peptide sequence within the EPO molecule, helix B surface peptide (HBSP), that possesses tissue-protective, but not erythropoietic properties of EPO, on mortality and cardiac remodeling in postmyocardial infarction-dilated cardiomyopathy in rats. Starting 2 weeks after permanent left coronary artery ligation, rats received i.p. injections of HBSP (60 mg/kg) or saline two times per week for 10 months. Treatment did not elicit an immune response, and did not affect the hematocrit. Compared with untreated rats, HBSP treatment reduced mortality by 50% (P , 0.05). Repeated echocardiography demonstrated remarkable attenuation of left ventricular dilatation (end-diastolic volume: 41 versus 86%; end-systolic volume: 44 versus 135%; P , 0.05), left ventricle functional deterioration (ejection fraction: 24 versus 263%; P , 0.05), and myocardial infarction (MI) expansion (3 versus 38%; P , 0.05). A hemodynamic assessment at study termination demonstrated normal preload independent stroke work (63 6 5 versus 40 6 4; P , 0.05) and arterioventricular coupling (1.2 6 0.2 versus 2.7 6 0.7; P , 0.05). Histologic analysis revealed reduced apoptosis (P , 0.05) and fibrosis (P , 0.05), increased cardiomyocyte density (P , 0.05), and increased number of cardiomyocytes in myocardium among HBSP-treated rats. The results indicate that HBSP effectively reduces mortality, ameliorates the MI expansion and CHF progression, and preserves systolic reserve in the rat post-MI model. There is also a possibility that HBSP promoted the increase of the myocytes number in the myocardial wall remote from the infarct. Thus, HBSP peptide merits consideration for clinical testing.

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“…Major putative mechanisms for the increase in blood pressure by repeated rHuEPO administration are expansion of blood volume, increased blood viscosity (4), and reversal of hypoxic vasodilatation (5). A direct vasoconstrictive effect of rHuEPO was also inferred from the results of an in vitro animal study in which vascular smooth muscle cells constricted in response to high concentrations of rHuEPO (10-200 U/ml) (6).…”

Section: Introductionmentioning

confidence: 99%

Blood Pressure Response to Erythropoietin Injection in Hemodialysis and Predialysis Patients

et al. 2004

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lin-1 (ET-1) (7). However, it is not well established whether rHuEPO increases blood pressure via ET-1 in patients on hemodialysis.Patients with chronic renal failure (CRF) and renal anemia are also treated with rHuEPO before the initiation of hemodialysis. In chronic renal failure patients, blood pressure often increases with the progression of renal failure via salt retention. Even though it has been reported that about 20% of predialysis CRF patients show an increase in blood pressure with rHuEPO therapy (8, 9), it is difficult to distinguish the erythropoietin-induced hypertension from the blood pressure increase associated with the progression of renal failure. In this study, we investigated the effect of a single injection of rHuEPO on blood pressure and ET-1 in patients receiving hemodialysis and in predialysis chronic renal failure patients.

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Effect of Treatment with Recombinant Human Erythropoietin on Peripheral Hemodynamics and Oxygenation

Cited by 67 publications

References 0 publications

Hypertension in Dialysis Patients

Hypertension in Dialysis Patients

Chronic Administration of Small Nonerythropoietic Peptide Sequence of Erythropoietin Effectively Ameliorates the Progression of Postmyocardial Infarction–Dilated Cardiomyopathy

Blood Pressure Response to Erythropoietin Injection in Hemodialysis and Predialysis Patients

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